Brain uptake of mannitol and sucrose after cerebral ischemia: effect of hyperglycemia.
The effect of 10 min cerebral ischemia on blood-brain barrier permeability to mannitol and sucrose was evaluated in normo- and hyperglycemic rats. In the period immediately after ischemia (1-4 min) the PS (permeability-surface area product) for mannitol was 159% +/- 75 of control (0.17 +/- 0.02 mg/100 g min) in the hyperglycemic rats (plasma glucose 8 mM) and 204% +/- 30 of control (0.09 +/- 0.02 mg/100 g min) in the hyperglycemic rats (plasma glucose 28 mM). Two hours after ischemia, PS for mannitol returned to the control levels in the normoglycemic rats and remained elevated in hyperglycemic animals. The mannitol/sucrose ratios-2.3 +/- 0.4 in normoglycemic rats and 2.6 +/- 0.1 in hyperglycemic rats-remained unchanged after ischemia. As there was no significant difference in the effects of ischemia on normo- and hyperglycemic rats, it was concluded that the deleterious effect of hyperglycemic on clinical recovery after cerebral ischemia in rats (Siemkowicz & Hansen 1978) is not related to enhancement of BBB damage.
D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000378:metabolism*; D008297:Male; D008353:Mannitol / Q000378:metabolism*; D010313:Partial Pressure; D051381:Rats; D013395:Sucrose / Q000378:metabolism*
D008353:Mannitol; D013395:Sucrose